The A2B receptor is overexpressed on various types of tumor cells and immune cells. A2B receptor expression and activation are regulated by hypoxia in the tumor microenvironment (TME) which causes immune suppression by inhibiting the activity of essential immune cells. Inhibiting A2B receptor prevents cancer cell proliferation in many solid tumor types including prostate and breast cancers.
Our first-in-class candidate, TT-702, works by making cancer more visible to the immune system so it can be destroyed.
TT-702 is in a Phase 1/2 clinical trial for the treatment of patients with a range of difficult-to-treat cancers including mCRPC, TNBC and MSI/MMR.
Compelling Pre-Clinical Data Supporting TT-702
TT-702 is Superior to Anti-PD-1 and Synergizes Anti-PD-1 Efficacy
TT-702 enhances the effect of anti-PD-1 in the hot tumor model
TT-702 is superior to anti-PD-1 in cold tumor model and combination with anti-PD-1 synergistically inhibits cold tumor growth
TT-702 Increases Key Immune Cells and Decreases Immunosuppressive Cells
TT-702 facilitates infiltration of CD4+ and CD8+ T cells and dendritic cells, and reduces regulatory t-cells (Tregs) and myeloid-derived suppressor cells (MDSCs)
TT-702 enhances the effect of anti-PD-1 on T cell infiltration and normalizes negative effect of anti-PD-1 on dendritic cells, Tregs, and MDSCs
TT-702 Inhibits Angiogenesis
TT-702 reduces VEGF production which could prevent angiogenesis, metastasis and tumor growth
TT-702 Inhibits Fibrosis
TT-702 reduces fibrosis which could prevent tumor metastasis and enhance response to immunotherapy
Teon’s rich pipeline targets unexploited metabolic pathways backed by well-validated science and a track record developing first- and best-in-class GPCR-directed therapies.